64. Acute adrenal insufficiency - etiology, pathogenesis, clinical manifestations.

Acute adrenal insufficiency – etiology, pathogenesis, and clinical manifestations.

Acute adrenal insufficiency (also called adrenal crisis or Addisonian crisis ) is a life-threatening condition caused by sudden, severe deficiency of adrenal corticosteroids, mainly cortisol ± aldosterone.

Etiology

1. 1 Sudden withdrawal of long- term corticosteroid therapy

Most common cause in developed countries.

Chronic steroid therapy suppresses hypothalamic-pituitary-adrenal (HPA) axis → adrenal atrophy → sudden stop leads to acute deficiency.

1. 2 Acute stress in patients with chronic adrenal insufficiency

Infection, trauma, surgery → sudden increased cortisol demand → crisis if adrenal reserve insufficient.

1. 3 Bilateral adrenal hemorrhage or infarction

Causes:

• Waterhouse-Friderichsen syndrome (usually in severe meningococcemia or sepsis → hemorrhagic necrosis of adrenal glands).
• Anticoagulant therapy.
• Trauma.
• Disseminated intravascular coagulation (DIC).

1. 4 Rapid destruction of adrenal glands

Autoimmune adrenalitis.

Metastases (e.g., from lung or breast cancer).

Pathogenesis

1. 1 Sudden drop in cortisol → impaired stress response.

Cortisol is critical for maintaining vascular tone, cardiac output, and glucose homeostasis.

1. 2 Aldosterone deficiency (if mineralocorticoid loss also occurs) →

Sodium loss → hyponatremia.

Potassium retention → hyperkalemia.

Volume depletion → hypovolemia → hypotension → shock.

1. 3 Hypoglycemia due to impaired gluconeogenesis.

Clinical manifestations

General symptoms

Severe weakness, fatigue.

Nausea, vomiting.

Abdominal pain (can mimic acute abdomen).

Fever.

Cardiovascular

Severe hypotension → shock.

Hypovolemia signs: cold, clammy skin.

Electrolyte disturbances

Hyponatremia → confusion, lethargy.

Hyperkalemia → muscle weakness, possible arrhythmias.

Hypoglycemia → sweating, tremors, confusion, coma.

Skin

In chronic underlying Addison disease: hyperpigmentation (due to high ACTH cross- reacting with melanocyte- stimulating hormone receptors).

In acute onset (e.g., hemorrhage ): no time for pigmentation changes.

Complications

Untreated → rapid progression to coma and death from circulatory collapse.

Summary Table